S100A2 Proteins, Antibodies, cDNA Clones Research Reagents

S100A2 (S100 Calcium Binding Protein A2) is a protein coding gene located on human chromosome 1q21.3. S100A2 is also known as CAN19 and S100L. The human S100A2 gene encodes a 11117 Da protein containing 98 amino acids. The S100A2 protein is biasedly expressed in esophagus, urinary bladder and other tissues. Among its related pathways are Direct p53 effectors. S100A2 is related to calcium ion binding and identical protein binding. S100A4 is an important paralog of S100A2 gene. S100A2 is associated with some diseases, including Conjunctival Intraepithelial Neoplasm and Pilomatrixoma.

S100A2 Protein (2)

    S100A2 Antibody (3)

      S100A2 cDNA Clone (15)

      S100A2 qPCR Primer (1)

      S100A2 Lysate (1)

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        S100A2 Background

        The calcium-binding protein S100A2 is a member of the S100 family of proteins containing 2 EF-hand calcium-binding motifs. S100 family genes are located as a cluster on chromosome 1q21, and S100 proteins consisting of at least 20 members are involved in the regulation of a number of cellular processes such as cell-cycle progression and cell differentiation. S100A2 was first detected in lung and kidney, and is mainly expressed in a subset of tissues and cells such as breast epithelia and liver. The S100A2 protein is a homodimer that undergoes a conformational change upon binding of calcium, and the active form functions in regulating cell proliferation and differentiation, gene transcription, and p53-dependent growth arrest and apoptosis. Accordingly, this protein is regarded as a putative tumor suppressor, and thus chromosomal rearrangements and reduced expression of S100A2 gene have been implicated in certain carcinomas.

        S100A2 References

        • Gimona, M. et al., 1997, J. Cell. Sci. 110: 611-621.
        • Mueller, A. et al., 2005, J. Biol. Chem. 280: 29186-29193.
        • Lapi, E. et al., 2006, Oncogene. 25: 3628-3637.
        • Feng, G. et al., 2001, Cancer. Res. 61: 7999-8004.
        • Gupta, S. et al., 2003, J. Clin. Oncol. 21: 106-112.

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